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Reinhard Heun

Publications and source records attributed to Reinhard Heun.

At least 19 recordsLinked to original sources

Identification of the genetic basis for complex disorders by use of pooling-based genomewide single-nucleotide-polymorphism association studies.

We report the development and validation of experimental methods, study designs, and analysis software for pooling-based genomewide association (GWA) studies that use high-throughput single-nucleotide-polymorphism (SNP) genotyping microarrays. We first describe a theoretical framework for establishing the effectiveness of pooling genomic DNA as a low-cost alternative to individually genotyping thousands of samples on high-density SNP microarrays. Next, we describe software called "GenePool," which directly analyzes SNP microarray probe intensity data and ranks SNPs by increased likelihood of being genetically associated with a trait or disorder. Finally, we apply these methods to experimental case-control data and demonstrate successful identification of published genetic susceptibility loci for a rare monogenic disease (sudden infant death with dysgenesis of the testes syndrome), a rare complex disease (progressive supranuclear palsy), and a common complex disease (Alzheimer disease) across multiple SNP genotyping platforms. On the basis of these theoretical calculations and their experimental validation, our results suggest that pooling-based GWA studies are a logical first step for determining whether major genetic associations exist in diseases with high heritability.

Alzheimer Disease↗

Familial aggregation of depression, but no familial aggregation of individual depressive symptoms.

BACKGROUND: Familial aggregation of major depression might indicate a genetic liability for the disorder. The complete disorder or, alternatively, only some individual symptoms might be inherited. Under the latter condition, an increased frequency of inherited symptoms might consecutively increase the likelihood to reach the threshold for depression in relatives and, thus, might cause the familial aggregation of depression. Up to now, no study investigated the possibility of a relationship between individual depressive symptoms and the familial aggregation of depression. METHODS: The familial aggregation of early-onset depression (age-at-onset < 60 years, EOD) but less so of late-onset depression (LOD) has been shown in this sample. To assess the hypothesis of an inheritance of individual depressive symptoms as a possible cause of the familial aggregation of depression, frequencies of symptoms were compared in relatives of depressed patients and of controls using forward logistic regression analyses. RESULTS: Some individual depressive symptoms showed clustering in relatives of patients with depression, but the pattern of inheritance was inconsistent, i.e. the clustering of symptoms was different between non-depressed and depressed relatives of patients with EOD and LOD, respectively. No intra-familial clustering of specific depressive symptoms within families of depressed subjects could be observed. CONCLUSIONS: Due to the inconsistencies in the clustering of individual symptoms in non-depressed and depressed relatives and the lack of intra-familial clustering, the familial aggregation of depression is unlikely to be caused by the aggregation of individual depressive symptoms. An inheritance of the vulnerability for complete depressive disorders influenced by environmental factors is more likely.

Age Factors↗

PPARD haplotype influences cholesterol metabolism but is no risk factor of Alzheimer's disease.

Cholesterol metabolism is involved in Alzheimer's disease (AD) pathogenesis: increased cholesterol blood levels are detected in AD patients, and treatment with statins reduces the risk of AD. The peroxisome proliferator-activated receptor delta protein (PPARdelta), is a member of the steroid hormone super family of ligand-inducible transcription factors, and is of major relevance in lipid and cholesterol metabolism. We investigated three frequent polymorphisms located in exons 4 (rs2016520) and 9 (rs3734254 and rs9794) of the PPARdelta gene (PPARD) for their putative influence on the risk of AD and on plasma levels of cholesterol, 24S-hydroxycholesterol and 27-hydroxycholesterol. The study population consisted of 167 AD patients (mean age: 74.27+/-9.37 years; female 78.6%) and 194 controls (mean age: 73.26+/-8.37 years; female 57.2%). Haplotype analysis was perfomed, however, we did not find PPARD haplotypes to influence the risk of AD. In contrast to these results, a two marker haplotype consisting of rs2016520 and rs9794 in AD patients showed a significant effect on the relative plasma levels of 24S-hydroxycholesterol (carriers: 32.1+/-2.8ng/mg; non-carriers: 40.3+/-1.4ng/mg; p=0.016) and 27-hydroxycholesterol (carriers: 40.8+/-7.7ng/mg; non-carriers: 58.6+/-2.3ng/mg; p=0.002) but not in non-demented controls. Our results suggest that PPARD haplotypes might influence levels of cholesterol metabolites in AD patients, but act not as risk factors of AD.

Aged↗

Successful verbal retrieval in elderly subjects is related to concurrent hippocampal and posterior cingulate activation.

OBJECTIVE: Memory decline and hippocampal atrophy are two major aspects of Alzheimer's disease. Using a response-related fMRI design, we investigated the relationship between successful verbal retrieval and concurrent cerebral activation in elderly subjects in different stages of cognitive decline. We chose a correlational over the more traditional categorical approach to increase the power of detecting relevant activations. METHODS: Eleven subjects with Alzheimer's disease, 21 elderly subjects with mild cognitive impairment, and 29 age-matched cognitively unimpaired subjects learned 180 nouns. While measuring brain activation with fMRI, the subjects had to classify these 180 learned plus 180 new distractor words as known or new. Response-related fMRI analysis was used to identify cerebral activation by correctly remembered words (hits) that correlated with retrieval success in the whole group. RESULTS: Successful verbal retrieval was significantly correlated with concurrent activation of the left hippocampus and posterior cingulate gyrus. CONCLUSION: The study confirms the importance of adequate hippocampal function for successful verbal retrieval in the elderly. In addition, our study supports connectivity studies indicating a functional relationship between the hippocampus and the posterior cingulate gyrus during successful verbal retrieval in the elderly in different stages of cognitive decline.

Aged↗

A functional polymorphism within plasminogen activator urokinase (PLAU) is associated with Alzheimer's disease.

A number of susceptibility loci for Alzheimer's disease (AD) have been identified including a region on Chromosome 10q21-q22. Within this region the plasminogen activator urokinase gene (PLAU) was considered as a reasonable candidate from its functional implication in plasmin generation, a serine protease capable of degrading beta-Amyloid (Abeta) protein. We screened 56 single nucleotide polymorphisms (SNPs) around PLAU using 1751 individuals from four independent case-control samples (Munich, N=679; Bonn N=282; Brescia (Italy) N=219; Perth (Australia) N=557 and one discordant sib-pair sample (Munich N=622). In brain tissue samples of neuropathologically confirmed cases with AD (N=33) we analyzed plaque counts according to the risk allele. We identified that one functional exonic SNP (rs2227564) is associated with development of AD using the four independent case-control samples (Munich, P=0.02; Bonn, P=0.005; Brescia (Italy), P=0.001; Perth (Australia), P=0.03) and the discordant sib-pair sample (P=0.001). In brain tissue, from neuropathologically confirmed cases with AD, we identified significantly higher plaque counts in carriers of the risk allele (N=6; 60.3+/-16.9) compared with non-carriers (N=9; 26.3+/-8.8; P=0.007). This study provides compelling evidence of a genetic and functional involvement of a common PLAU variant into the pathogenesis of AD. Further functional investigations are warranted to elucidate the specific role of PLAU, respectively, PLAU variants in the metabolism of Abeta proteins.

Age of Onset↗

Association of polymorphism in the transcription factor LBP-1c/CP2/LSF gene with Alzheimer's disease and major depression.

The transcription factor LBP-1c/CP2/LSF (LBP-1c) is a candidate gene for Alzheimer's disease (AD) because it is located in a putative hotspot for an AD risk gene on chromosome 12. We investigated the effect of LBP-1c polymorphism on the risk of AD in 162 AD patients, 180 patients with major depression as hospitalized controls and 225 healthy subjects. We observed no significant association of the LBP-1c A allele with AD. Nor did we detect an interaction of the LBP-1c A allele with the apolipoprotein E4 (ApoE4) allele or the low-density lipoprotein receptor-related protein T allele which could have been related to the risk of AD. However, exploratory data analysis revealed that the LBP-1c A allele might act as a protective factor in major depression. A recent study also described an association of another gene located on chromosome 12, the mannose 6-phosphatase receptor gene, with major depression. These data suggest the presence of a putative risk gene for major depression at chromosome 12.

Aged↗

Mild cognitive impairment (MCI) and actual retrieval performance affect cerebral activation in the elderly.

Cerebral activation in the elderly may depend on general cognitive decline as well as actual retrieval performance. Consequently, activation between subjects with and without Mild Cognitive Impairment (MCI), and between remembered and non-remembered words was compared. Twenty-one MCI and 29 healthy control subjects learned 180 nouns. During retrieval, subjects had to discriminate these and 180 distractor words. fMRI identified response-related activation. Most retrieval-related activation was comparable in both groups. However, MCI subjects showed more activation in the prefrontal cortex than controls during processing of hits and correct rejections. Hits showed increased activation than misses in the precuneus and left lateral parieto-occipital cortex; misses showed more activation than correct rejections in the precuneus to cuneus. Verbal retrieval activated a large common network in the elderly independently of MCI. Increased activation in MCI subjects in prefrontal cortex depends on response category. Activation differences between response categories might reflect success (hits) and effort (misses). Increased retrieval-related activation may be used as early marker in subjects at risk of Alzheimer's disease.

Aged↗

A multicenter reproducibility study of single-voxel 1H-MRS of the medial temporal lobe.

Proton magnetic resonance spectroscopy ((1)H-MRS) has provided evidence for a reduction of N-acetyl-aspartate (NAA) in the medial temporal lobe (MTL) in cerebral disorders such as Alzheimer's Disease. Within the (1)H-MRS study of the German Research Network on Dementia, we determined the multicenter reproducibility of single-voxel (1)H-MRS of the MTL. At five sites with 1.5T MR systems, single-voxel (1)H spectra from the MTL of an identical healthy subject were measured. The same subject was also examined at one of the sites five times to assess intracenter stability. The protocol included water-suppressed spectra with TE 272 ms and TE 30 ms and unsuppressed spectra for absolute quantification of metabolite concentrations. The intracenter reproducibility of absolute NAA concentration, expressed as coefficient of variation (CV), was 1.8%. CV for the concentrations of creatine (Cr), choline (Cho), and myoinositol (MI) and for the ratios NAA/Cr, NAA/Cho, and MI/NAA varied by 11-16%. Intercenter CV was 3.9% for NAA and were below 10% for all other metabolites and metabolic ratios. Our study demonstrates that quantitative assessment of NAA with single-voxel MRS can be performed with high intercenter reproducibility. This is the basis for applying (1)H-MRS in large-scale early recognition and treatment studies in MTL affecting disorders.

Adult↗

Polymorphism in ABCA1 influences CSF 24S-hydroxycholesterol levels but is not a major risk factor of Alzheimer's disease.

The ATP-binding cassette transporter A1 (ABCA1) mediates reverse cholesterol transport, polymorphisms have been shown to influence the levels of cholesterol and of HDL and the risk of coronary artery disease. Since altered cholesterol metabolism is also involved in Alzheimer's disease (AD), the effects of two ABCA1 polymorphisms (G-395C promoter polymorphism (rs 2246293) and exonic R219K) on the risk of AD in 241 AD patients and 294 non-demented controls, and on CSF cholesterol and 24S-hydroxycholesterol in 74 AD patients and 42 non-demented controls were investigated. None of the investigated ABCA1 polymorphisms influenced the risk of AD. However, the ABCA1 G-395C polymorphism influenced CSF levels of 24S-hydroxycholesterol, but not of cholesterol, whereas the R219K influenced neither CSF levels of 24S-hydroxycholesterol nor cholesterol. Our data support the observation that ABCA1 polymorphisms influence cholesterol metabolism of the brain, but might not act as a major risk factor in AD.

ATP Binding Cassette Transporter 1↗

Volume reduction of the entorhinal cortex in subjective memory impairment.

To examine the biological basis of subjective memory impairment (SMI), defined as the feeling of memory worsening with normal memory performance, we measured the volume of the entorhinal cortex (EC) and the hippocampus in SMI subjects, patients with mild cognitive impairment (MCI), patients with Alzheimer's disease (AD) and healthy controls (CO). Compared with controls, the EC was smaller in the SMI group (left: p=0.060; right: p=0.045) and in the other two groups in the following order: CO>SMI>MCI>AD. The same sequence was observed with regard to hippocampal volumes, but the volume reduction of the left hippocampus in the SMI group only reached a trend towards significance (p=0.072) and the right was not significantly smaller compared with controls (p=0.37). Compared with controls the average (left/right) volume reduction of the EC was 18% (SMI), 26% (MCI) and 44% (AD). The mean volume reduction of the hippocampus was 6% (SMI), 16% (MCI) and 19% (AD). Our results mirror the temporal sequence of neurodegeneration in AD and support the concept of SMI as the first clinical manifestation of dementia.

Aged↗

A comparative study of the different N-acetylaspartate measures of the medial temporal lobe in Alzheimer's disease.

OBJECTIVE: To investigate group differences and correlations and to determine the sensitivity and specificity of different measures of the neuronal marker N-acetylaspartate (NAA) in the medial temporal lobe of Alzheimer's Disease (AD) patients. METHODS: The metabolic ratio NAA/creatine (Cr), the absolute concentration of NAA referenced against brain tissue (BT) water and NAA multiplied with the amount of BT in the proton magnetic resonance spectroscopy (1H-MRS) voxel were assessed in patients and healthy controls with a single-voxel 1H-MRS protocol. RESULTS: All measures were significantly lower in AD patients compared with controls. NAA/Cr and NAA correlated weakly, and there was no correlation of NAA with the amount of BT in the voxel. The highest specificity (87%) at a sensitivity of 80% was observed for NAA multiplied with the amount of BT in the voxel. There was no correlation of the MMSE with any of the NAA parameters. CONCLUSIONS: NAA/Cr does not reflect NAA concentration very well. NAA is not correlated with brain atrophy. The BT volume in the 1H-MRS voxel in combination with the concentration of NAA discriminates AD from healthy controls sufficiently.

Aged↗

Risk factors and early signs of Alzheimer's disease in a family study sample. Risk of AD.

OBJECTIVE: Several predictors of Alzheimer's disease (AD) have been identified. However, the relevance and independent contribution of risk factors and of possible early signs such as mild cognitive impairment and subjective memory impairment on the development of AD has not been investigated prospectively in a cohort of non-demented elderly including first-degree relatives of AD subjects. METHOD: The development of AD was investigated in 757 non-demented elderly. Initial diagnoses were made from personal interviews. Information on 633 subjects after 4.7 +/- 1.2 years (mean +/- SD) was obtained either from personal or family history interviews. Using forward logistic regression analysis, predictors were identified by comparing their presence in 38 subjects who developed AD and 577 subjects who remained non-demented. RESULTS: The most important predictors of later Alzheimer's disease were increased age (Odds ratio OR = 1.086/additional year, p < 0.001), initial subjective memory complaints (OR = 2.68, p = 0.019), initial mild cognitive impairment (OR = 2.51, p = 0.032) and female gender (OR = 2.84, p = 0.069). Exploratory analysis revealed that previous depression after the age of 60 years (OR = 2.37, p = 0.033) and the presence of the apolipoprotein E4 allele (OR = 2.49, p = 0.043) individually predicted new AD during follow-up. A positive family history of AD (i. e. being a first degree relative of a subject suffering from AD) did not significantly influence the development of AD (p > 0.2). CONCLUSIONS: Increased age, the presence of mild cognitive impairment, subjective memory impairment and gender are the most relevant independent predictors of later Alzheimer's disease that may be used in combination for clinical prediction of AD.

Age Factors↗

The power of sample size and homogenous sampling: association between the 5-HTTLPR serotonin transporter polymorphism and major depressive disorder.

BACKGROUND: Several lines of evidence indicate that abnormalities in the functioning of the central serotonergic system are involved in the pathogenesis of affective illness. A 44-base-pair insertion/deletion polymorphism in the 5' regulatory region of the serotonin transporter gene (5-HTTLPR), which influences expression of the serotonin transporter, has been the focus of intensive research since an initial report on an association between 5-HTTLPR and depression-related personality traits. Consistently replicated evidence for an involvement of this polymorphism in the etiology of mood disorders, particularly in major depressive disorder (MDD), remains scant. METHODS: We assessed a potential association between 5-HTTLPR and MDD, using the largest reported sample to date (466 patients, 836 control subjects). Individuals were all of German descent. Patients were systematically recruited from consecutive inpatient admissions. Control subjects were drawn from random lists of the local Census Bureau and screened for psychiatric disorders. RESULTS: The short allele of 5-HTTLPR was significantly more frequent in patients than in control subjects (45.5% vs. 39.9%; p = .006; odds ratio = 1.26). CONCLUSIONS: These results support an involvement of 5-HTTLPR in the etiology of MDD. They also demonstrate that the detection of small genetic effects requires very large and homogenous samples.

Adult↗

APOA1 polymorphism influences risk for early-onset nonfamiliar AD.

Alterations in cholesterol homeostasis influence the risk for Alzheimer's disease (AD). Apolipoprotein A1 is the major apolipoprotein of the high-density lipoprotein and is involved in reverse cholesterol transport. Variation in the apolipoprotein A1 gene (APOA1) might influence the function of the protein, and thus brain cholesterol metabolism, leading to an increased risk for AD. Two polymorphisms of APOA1, a G/A substitution at position -75bp and a C/T and G/A base substitution at position +83bp or +84bp, or both, in the APOA1 promoter, have been described. We investigated the effect of these polymorphisms on the risk for AD in 427 AD patients and 500 healthy control subjects of German and English descent. The A allele of the APOA1 -75bp G/A polymorphism was associated with an increased risk for AD in subjects with an age at onset of 66 years or younger. Further data analysis indicated that AD patients homozygous for the A allele at position -75bp presented with disease onset 8 years earlier than carriers of at least one G allele. No influence of the +83/84bp polymorphism on the risk for AD was observed. These results suggest that variants of APOA1 might influence the onset and the risk for AD.

Age of Onset↗

Suicide attempts in schizophrenia and affective disorders with relation to some specific demographical and clinical characteristics.

Demographical and clinical characteristics have been reported to modulate the risk for suicide. This study analysed demographical and clinical characteristics with respect to lifetime suicide attempts in 500 individuals affected with schizophrenic or affective disorders. Suicide attempts were associated with poor premorbid social adjustment, low age at onset, low scores on the "Global Assessment Scale" and childlessness in females.

Adult↗

Risk factors of major depression in the elderly.

BACKGROUND: Several risk factors of depression have been identified in retrospective as well as some prospective studies in the elderly. Confirmation in independent samples is needed. The present follow-up study prospectively investigated risk factors of depression in an elderly German sample. METHODS: One thousand four hundred and thirty-one subjects from a family study were re-investigated after 4.7 +/- 2.5 years. Bivariate and multivariate forward logistic regression analyses were used to identify risk factors of the development of new depression in the elderly. RESULTS: Risk factors of a new depressive episode in 1408 elderly without current depression were age, female gender, a previous depression, subjective memory impairment, previous anxiety and somatoform disorders. The presence of dementia or mild cognitive impairment were significant risk factors in bivariate, but not multivariate analysis controlling for possible confounding. Risk factors of a first geriatric depressive episode were age, gender and subjective memory impairment; age remained the only significant risk factor in multivariate analysis. CONCLUSIONS: This investigation confirms previous studies from other countries concerning the relevance of risk factors for depression in the elderly. The knowledge of risk factors might help identify subjects at increased risk of depression for early intervention approaches. Elderly with a history of previous depression carry the highest risk.

Age Distribution↗